cocaine/hypoxia

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Hypoxia after prenatal cocaine attenuates striatal dopamine and neurotrophic activity.

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We have previously shown that newborn rabbits exposed to cocaine prenatally have an altered cardiorespiratory response to hypoxia. We report the effect of postnatal hypoxia on brain DA and neurotrophic activity in New Zealand White rabbit pups (n = 41) born to cocaine-exposed does (30 mg/kg/day SC

Decreased ventilatory response to hypoxia in sedated newborn piglets prenatally exposed to cocaine.

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OBJECTIVE Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets. METHODS Cocaine

Prenatal cocaine alters diaphragmatic EMG responses to hypoxia in developing swine.

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To distinguish pure effects of prenatal cocaine exposure on respiratory control from confounding factors inherent to drug abuse, a porcine model was established. Cocaine was administered at 2 mg/kg 4 times daily during 0.66-1.0 gestation to 5 paired sows. At birth, cocaine-exposed piglets were

Brain damage and hypoxia in an ovine fetal chronic cocaine model.

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OBJECTIVE To assess the development of brain damage in an ovine fetal chronic cocaine model. To evaluate the effect of isolated hypoxic tests on this model and to correlate hemodynamic findings (brain-sparing effect) following fetal hypoxia and the occurrence of brain damage. METHODS Fifteen ewes

Effects of prenatal cocaine on the ventilatory response to hypoxia in newborn rabbits.

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Recently, investigators have reported an alteration of postnatal respiratory pattern, deficient hypoxic arousal from sleep, and an increased incidence of sudden infant death syndrome (SIDS) among human infants exposed to cocaine prenatally, thus suggesting that prenatal cocaine exposure may perturb

Effect of cocaine in early gestation. Physiologic responses to hypoxia in newborn rabbits.

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To investigate the effect of prenatal cocaine on the physiologic responses to hypoxia, we evaluated ventilation, oxyhemoglobin saturation, and pulse rate at 0.21 FIO2 (baseline) and in response to 20-min exposure to either 0.15 or 0.08 FIO2 on Days 4 to 6 of life in 31 unanesthetized New Zealand

Cocaine exacerbates hypoxia-induced cell damage in the developing brain: effects on ornithine decarboxylase activity and protein synthesis.

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The immature brain is resistant to cell damage from hypoxia, such as that experienced during parturition. Because cocaine causes cerebral ischemia, we examined whether cocaine interferes with this resistance. On postnatal days 1, 4 or 8, neonatal rats were given an acute injection of saline or

Prenatal cocaine exposure and postnatal hypoxia independently decrease carotid body dopamine in neonatal rats.

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The effects of prenatal cocaine exposure on the levels of carotid body dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were investigated in 5-day-old rat pups exposed to normoxic and hypoxic conditions. Timed-pregnant Sprague-Dawley rats were

Cocaine added to heroin fails to affect heroin-induced brain hypoxia

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Heroin and cocaine are both highly addictive drugs that cause unique physiological and behavioral effects. These drugs are often co-administered and cocaine has been found in ~20% of cases of opioid overdose death. Respiratory depression followed by brain hypoxia is the most dangerous effect of

Neuroimaging of hypoxia and cocaine-induced hippocampal stroke.

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The hippocampus has been a subject of numerous studies of behavior and memory in patients who demonstrate atrophy, sclerosis, or injury by autopsy or imaging. It has also been studied in patients who undergo surgical treatment for intractable epilepsy. The effects of hypoxia and ischemia on the

Reactive Oxygen Species/Hypoxia-Inducible Factor-1α/Platelet-Derived Growth Factor-BB Autocrine Loop Contributes to Cocaine-Mediated Alveolar Epithelial Barrier Damage.

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Abuse of psychostimulants, such as cocaine, has been shown to be closely associated with complications of the lung, such as pulmonary hypertension, edema, increased inflammation, and infection. However, the mechanism by which cocaine mediates impairment of alveolar epithelial barrier integrity that

Protection against cerebral hypoxia by local anesthetics: a study using brain slices.

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The ability of the local anesthetics lidocaine, 2-chloroprocaine and cocaine to protect neuronal tissue against hypoxic damage was evaluated. Rat hippocampal slices were incubated with non-depressive doses of these agents 60 min prior to their exposure to 15 min hypoxia. The rate of recovery of

CNS complications of cocaine abuse: prevalence, pathophysiology, and neuroradiology.

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The United States is facing an epidemic of cocaine use by adolescents and young adults from all socioeconomic backgrounds. Epidemiologic data suggest that the use of the drug continues to increase on a year-by-year basis. This is a serious public health problem because cocaine is highly addictive

Antenatal smoking and substance-misuse, infant and newborn response to hypoxia.

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OBJECTIVE To determine at the peak age for sudden infant death syndrome (SIDS) the ventilatory response to hypoxia of infants whose mothers substance misused in pregnancy (SM infants), or smoked during pregnancy (S mothers) and controls whose mothers neither substance misused or smoked. In addition,

Hypoxia and the Edema Syndrome: elucidation of a mechanism of teratogenesis.

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The elucidation of mechanisms and pathogenesis of birth defects is exceedingly complex. Consequently, there are few examples where the etiology of birth defects caused by a specific agent has been well described. One such example is the "Edema Syndrome" first described by Casimer Grabowski in the

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